Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of depletion of p53 and BACH1 on gene expression in human tongue squamous cell carcinoma cell line Cal-33.

ABSTRACT: To investigate how BACH1 and p53-R175H regulate metastasis-related genes, we transiently transfected Cal-33 cells with control or p53 or BACH1 siRNA to knock down these genes expression. We then performed gene expression profiling analysis using data obtained from RNA-seq of these knockdown cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE224730 | GEO | 2023/02/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of depletion of p53 and BACH1 on gene expression in human tongue squamous cell carcinoma cell line Cal-33.

Project description:Effect of depletion of p53 and BACH1 on gene expression in human tongue squamous cell carcinoma cell line Cal-33.

| PRJNA932318 | ENA

Genome-wide map of BACH1 binding in HEK 293T cells

Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of BACH1 target genes in HEK 293 cells with knock-down of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by ChIP-seq were found highly enriched in genes showing expression changes after BACH1 knock-down, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, SLC48A1) and redox regulation (GCLC, GCLM, SLC7A11), we also discovered BACH1 target genes effecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis. Examination of BACH1 binding in HEK 293T cells by chromatin immunoprecipitation-sequencing (CHIP-seq) with input DNA as control.

2011-05-13 | E-GEOD-28051 | biostudies-arrayexpress

BACH1-AS1

Project description:Homo sapiens BACH1-AS1, BACH1 antisense RNA 1 [Source:HGNC Symbol;Acc:HGNC:40008], is expressed in 33 baseline experiment(s);

| ENSG00000232118 | ExpressionAtlas

BACH1-AS1

Project description:Homo sapiens BACH1-AS1, BACH1 antisense RNA 1 [Source:HGNC Symbol;Acc:HGNC:40008], is differentially expressed in 9 experiment(s);

| ENSG00000232118 | ExpressionAtlas

Role of BACH1 in HEK 293T cells

Project description:This SuperSeries is composed of the following subset Series: GSE28050: Expression data from knockdown of BACH1 in HEK 293T cells GSE28051: Genome-wide map of BACH1 binding in HEK293T cells Refer to individual Series

2011-05-12 | E-GEOD-28053 | biostudies-arrayexpress

Dual BACH1 regulation by complementary SCF-type E3 ligases

Project description:BACH1, FBXO22, FBXL17, oxidative stress response, E3, Cullin-RING ligases, F-box, cysteine modification, S-nitrosylation, heme

2024-12-03 | PXD051074 | Pride

Regulation of immunity by Bach1 in Mice

Project description:Genes regulated by Bach1 transcription factor

2012-07-09 | E-MEXP-3674 | biostudies-arrayexpress

BACH1 as a master regulator gene in vascular cells during aging

Project description:We identify transcription factor BACH1 as a master regulator in vascular cells during aging. BACH1 is upregulated in the aorta of old mice. We find BACH1 is located on open chromatin and BACH1 binds to CDKN1A gene enhancer and activates its transcription in endothelial cells. Finally, BACH1 aggravates endothelial cell senescence under oxidative stress. Thus, these findings demonstrate a crucial regulatory role of BACH1 in vascular aging.

2024-09-15 | GSE185210 | GEO

Genome-wide map of BACH1 binding in HEK 293T cells

2011-05-13 | GSE28051 | GEO

Human glioblastoma cells: Tet-on(mutant p53 R175H expression) vs Tet-off(p53-null)

Project description:TP53 R175H mutation is one of the most common mutations in human cancers and cancer cells with this mutation stably express R175H protein in the nucleus. To identify the synthetic lethal gene interacted with the R175H, we conducted the high throughput screening by using tetracyclin inducible R175H expression system in SF126 cells and comprehensive shRNA library carried by lenti virus. We identified 906 candidate gene suppressions that may lead to accelerated cell growth inhibition under the presence of R175H. Inhibitor of differentiation 1 (ID1) was one of the candidate genes and suppression of ID1 by siRNA resulted in acceleration of growth inhibition of cell lines expressing endogenous R175H but not in TP53 null cell lines. The transient expression of R175H in TP53 null cell lines and suppression of ID1 and/or TP53 R175H in cell lines with endogenous R175H revealed that the cell growth inhibition by ID1 suppression was dependent on R175H expression but not other common p53 mutants (R273H). Flow cytometric (FACS) analysis exhibited that ID1 suppression resulted in G1 arrest and the arrest was accelerated by suppression of R175H. In conclusion, ID1 is a synthetic lethal gene interacted with R175H and is considered to be a novel molecular target of cancer therapy for R175H expressing cells. R175H expression(Tet-on) group was labeled by Cy5, and p53-null(Tet-off) group was labeled by Cy3. Three independent experiments were conducted (We have triplicate data).

2011-11-02 | E-GEOD-33362 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data